Working with mice, scientists at the Washington University School of Medicine in St. Louis (WUSL) say that the herpes virus can assist the immune system in fighting-off various harmful bacteria. The surprising finding, reported in Nature, suggests that our bodies may develop a symbiotic relationship with the virus and that other viruses may also affect how our bodies respond to pathogens.

Herpes viruses include oral and genital herpes, chickenpox, cytomegalovirus, Epstein-Barr virus and Kaposi's sarcoma. Typically, symptoms like fever, cold sores or blisters can occur before the virus enters periods of latency. The virus then remains dormant although it can flare up again, usually in response to stress or ill-health.

WUSL researcher, Herbert W. "Skip" Virgin, said that he was studying how mouse herpes viruses transitioned from acute to latent infections when he became interested in the possibility that latent infections might confer unrecognized benefits. "We found evidence that the mouse immune system controls latent herpes infections in part by increasing production of a protein hormone called interferon gamma," Virgin explained. "This is a signaling hormone that in effect puts some immune system soldiers on yellow alert, causing them to patrol for invaders with their eyes wide open and defense weapons ready."

Virgin and co-researcher Erik Barton tested herpes-infected mice with exposure to two bacteria: Yersinia pestis, which causes plague, and Listeria monocytogenes, which causes food poisoning. The researchers found that when mice had a latent herpes infection, the bacteria replicated more slowly and were less likely to kill the mice.

Virgin suspects that the virus may be prompting the immune system to produce more interferon gamma to keep itself from emerging from latency. If the virus stays latent, it prevents itself from seriously endangering the host and can continue to spread to new hosts.

The new study could have wide-reaching implications for immune research. Humans have spent millions of years living and evolving with latent viral infections and the new results imply that infections may have fundamentally altered our immune systems. This could mean the virus-free animal models scientists use to study vaccines and diseases may be producing misleading research results.

Stressing that they did not want to disregard the human suffering and health risks caused by disease-causing herpes infections, the researchers nevertheless suggested that future studies should look at whether humans receive similar advantages from other chronic infections. "Chronic virus infections may in part define what a normal human immune response is," said Virgin.